Congenital Lobar Emphysema Developing Massive Hemoptysis in Adulthood Treated by Thoracoscopic Lobectomy.

Congenital lobar emphysema (CLE) is a rare developmental lung disorder characterized by lobar hyperinflation secondary to bronchopulmonary obstruction. Half of patients are symptomatic at birth, with many requiring urgent or emergent surgical resection to treat respiratory distress. Meanwhile, patients achieving late childhood or adolescence without symptoms usually never require surgery. We present a case of a 26 year old otherwise healthy female with known CLE who developed massive hemoptysis and required urgent videoscopic (VATS) resection of her right lung upper lobe. We know of no other report of CLE causing life-threatening bleeding at any age, and herein review pathology and pathophysiology of the condition.

Saved by the Scan: A Case of Early Detection of Sarcomatoid Mesothelioma.

We report a case of localized sarcomesothelioma detected during screening via a low-dose CT (LDCT) scan. The patient is a 71-year-old female, a current 56-pack-year cigarette smoker with a past medical history of myocardial infarction and stroke with a Zubrod score of zero. A screening LDCT revealed a 1.9 cm × 1.8 cm × 1.4 cm right lower lobe lesion with smooth margins and close association with the hemidiaphragm. A wedge resection with biopsy showed high-grade sarcomatoid mesothelioma with extensive desmoplastic morphology and negative margins. The patient opted for imaging surveillance, and at 12 months has shown no evidence of tumor recurrence on positron emission tomography (PET)/CT. The case shows that LDCT screening discovers cancers and saves lives. It also presented a dilemma for the patient and her oncologist because common guidelines do not define a recommended treatment.

Thoracoscopic transmyocardial laser revascularization: is prior coronary artery bypass grafting a contraindication?

OBJECTIVE: : Recently, thoracoscopic techniques have been used to perform transmyocardial laser revascularization (TMR) in patients who are not suitable candidates for coronary artery bypass graft (CABG) surgery or percutaneous coronary interventions. Whether or not prior CABG contraindicates a port access-only approach to TMR is unclear. This study compares patients with and without prior CABG who have undergone thoracoscopic TMR. METHODS: : Between May 2003 and October 2005, 23 consecutive patients (6 without prior CABG, group A; and 17 with prior CABG, group B) underwent thoracoscopic TMR, using a holmium:yttrium-aluminum-garnet (Ho:YAG) laser system. Either 3 or 4 port incisions (each ≤2 cm in length) were used, depending on the patient's anatomy. Procedural success was defined as the ability to create all intended channels without conversion to thoracotomy. RESULTS: : Patient demographics were not significantly different between group A and group B (mean age, 65.8 ± 4.3 years versus 67.4 ± 2.4 years, Canadian Cardiovascular Society angina class 3.7 ± 0.2 versus 3.9 ± 0.1, and Parsonnet score 12.0 ± 3.2 versus 20.5 ± 2.4). Fourteen (82.4%) group B patients had a prior left internal mammary artery to left anterior descending artery graft, of which 12 (85.7%) were patent. One patient in group A had an airway injury at intubation that led to an extended hospital stay of 30 days. One patient in group A (16.7%) and one patient in group B (5.9%) required a blood transfusion (P = NS). Adhesion lysis time in group B ranged from 0 to 68 minutes (mean, 27 ± 5.6 minutes). Neither group had a conversion to thoracotomy or any deaths through a mean combined follow-up of 12 months. CONCLUSIONS: : A port access approach is safe and reproducible for patients who are candidates for sole therapy TMR. Prior CABG, including patent grafts, is not a contraindication to thoracoscopic TMR.

Axillary cannulation for proximal aortic surgery is as safe in the emergent setting as in elective cases.

BACKGROUND: Right axillary artery cannulation and selective antegrade cerebral perfusion (SCP) have become well-described strategies in the surgical treatment of proximal aortic disease. Many series report increases in adverse outcomes with SCP used in emergent settings. We compare outcomes in elective and emergent patients. METHODS: Over 21 months, SCP through right axillary cannulation with a side graft was performed in 61 patients. Thirty-three percent (20 of 61) underwent emergent operation for Stanford type A dissection or intramural hematoma, including 3 of 20 (4.7%) with pericardial tamponade; the remainder of SCP (41 of 61) was elective. The mean follow-up was 9.1 +/- 0.40 months. RESULTS: Selective antegrade cerebral perfusion was used in 20 of 22 emergent cases (91%), with 2 unsuccessful cannulation attempts, and no peripheral arterial dissections encountered. The SCP flows averaged 16.3 +/- 0.71 cc x kg(-1) x min(-1) for a mean perfusion period of 26.1 +/- 1.9 minutes. The average cardiopulmonary bypass time for all patients was 173 +/- 11 minutes. Average hospital stay was 8.1 +/- 0.80 days. One case (1.3%) of permanent and 3 cases (4.8%) of temporary neurologic dysfunction occurred in SCP patients. The hospital mortality rate for emergent SCP cases (2 of 20, 10%) was not statistically different from the mortality rate for elective SCP cases (3 of 41, 7.3%, p = not significant), with no difference in complication rates. All 3 SCP patients with preoperative tamponade survived without complication. Cerebral oximetry data showed a trend toward decreased left-sided (contralateral) scalp perfusion. There was no association of emergent status with neurologic dysfunction, death, or any other adverse outcome. CONCLUSIONS: Axillary cannulation and SCP in the surgical treatment of proximal aortic pathology is safe in both elective and emergent settings.

Reduction of infarct size and preservation of endothelial function by multidose intravenous adenosine during extended reperfusion.

It has been proposed that infarct extension is developed from the early to the late phase of reperfusion (R). This study compares the protective effect of single or multidose administration of adenosine (Ado) on infarct size during early and late phases of R by attenuating neutrophil (PMN) recruitment. Forty-one dogs underwent 60-min left anterior descending artery (LAD) ischemia followed by 6, 24, and 48 h of R, respectively. Infarct size (%) increased over 6 to 24 h (27 +/- 2 to 38 +/- 4; P < 0.05 24 h versus 6 h group), with a corresponding increase in creatine kinase activity. Transmural myocardial blood flow (mL/min/g) decreased from 6 to 24 h (0.47 +/- 0.02 to 0.29 +/- 0.02; P < 0.05 24 h versus 6 h group). PMN localization (mm(2) myocardium) in the perinecrotic tissue detected by immunohistochemistry with anti-CD18 antibody, and accumulation detected by myeloperoxidase (MPO, DeltaAbs/min/g) increased from 6 to 24 h (292 +/- 25 to 605 +/- 44; P < 0.05 24 h versus 6 h group; and 55 +/- 7 to 96 +/- 5; P < 0.05 24 h versus 6 h group), respectively. In in vitro analysis, PMN adherence (mm(2) endothelium) to postischemic LAD increased from 98 +/- 2 to 125 +/- 3 (P < 0.05 24 h versus 6 h group) and maximal LAD endothelium-dependent relaxation (%) impaired from 6 to 24 h (74 +/- 7 to 42 +/- 10; P < 0.05 24 h versus 6 h group). Intravenous Ado (140 microg/kg/min) for 2 h at R reduced infarct size (17 +/- 2; P < 0.05 Ado versus 6 h group), CD18 positive cells (130 +/- 10; P < 0.05 Ado versus 6 h group), MPO (14 +/- 3; P < 0.05 Ado versus 6 h group), PMN adherence (57 +/- 2; P < 0.05 Ado versus 6 h group), and augmented LAD vascular relaxation (102 +/- 5 versus 74 +/- 7; P < 0.05 Ado versus 6 h group). However, this protection by Ado was lost when R was extended to 24 h. Treatment with multiple infusion of Ado at 2, 6, 12, and 18 h R significantly preserved protective effects seen at 6 h R in the Ado group. Protection by multidose Ado was still preserved when R was extended to an additional 24 h. These data suggest that interventions aiming at permanently reducing R injury may thus need to be administered not only at early R, but also during late phase. A slow wave of PMN accumulation at late R may be involved in the extension of infarction and endothelial dysfunction.

Pretreatment with phenoxybenzamine attenuates the radial artery's vasoconstrictor response to alpha-adrenergic stimuli.

BACKGROUND: Although the radial artery bypass conduit has excellent intermediate-term patency, it has a proclivity to vasospasm. We tested the hypothesis that brief pretreatment of a radial artery graft with the irreversible adrenergic antagonist phenoxybenzamine attenuates the vasoconstrictor response to the vasopressors phenylephrine and norepinephrine compared with the currently used papaverine/lidocaine. METHODS: Segments of human radial artery grafts were obtained after a 30-minute intraoperative pretreatment with a solution containing 20 mL of heparinized blood, 0.4 mL of papaverine (30 mg/mL), and 1.6 mL of lidocaine (1%). The segments were transported to the laboratory and placed into a bath containing Krebs-Henseleit solution and 10, 100, or 1000 micromol/L phenoxybenzamine or vehicle. The segments were tested in organ chambers for contractile responses to increasing concentrations of phenylephrine and norepinephrine (0.5-15 micromol/L). RESULTS: Contractile responses to 15 micromol/L phenylephrine in control radial artery segments averaged 44.2% +/- 9.1% of the maximal contractile response to 30 mmol/L KCl. Papaverine/lidocaine modestly attenuated contraction to 15 micromol/L phenylephrine (32.1% +/- 5.9%; P =.22), but 1000 micromol/L phenoxybenzamine completely abolished radial artery contraction (-7.2% +/- 4.4%; P <.001). The effect of 10 and 100 micromol/L phenoxybenzamine on attenuating vasocontraction was intermediate between 1000 micromol/L phenoxybenzamine and papaverine/lidocaine. Responses to 15 micromol/L norepinephrine in control radial artery segments averaged 54.7% +/- 7.5% of maximal contraction to 30 mmol/L KCl. Papaverine/lidocaine modestly attenuated the contraction response of radial artery segments (35.6% +/- 5.1%; P =.04). In contrast, 1000 micromol/L phenoxybenzamine showed the greatest attenuation of norepinephrine-induced contraction (-10.5% +/- 2.0%; P <.001). CONCLUSIONS: A brief pretreatment of the human radial artery bypass conduit with 1000 micromol/L phenoxybenzamine completely attenuates the vasoconstrictor responses to the widely used vasopressors norepinephrine and phenylephrine. Papaverine/lidocaine alone did not block vasoconstriction to these alpha-adrenergic agonists.

Optimal dose and mode of delivery of Na+/H+ exchange-1 inhibitor are critical for reducing postsurgical ischemia-reperfusion injury.

BACKGROUND: In clinical trials, perioperative intravenous Na(+)/H(+) exchange isoform-1 (NHE1) inhibitors were only moderately effective in high-risk patients undergoing surgical reperfusion (GUARDIAN trial). However, effective myocardial concentrations of NHE1 inhibitor may not have been achieved by parenteral administration alone. We tested the hypothesis that increasing doses of NHE1 inhibitor EMD 87580 ((2-methyl-4,5-di-(methylsulfonyl)-benzoyl)-guanidine) delivered in blood cardioplegia (BCP) and by parenteral route at reperfusion reduce myocardial injury after surgical reperfusion of evolving infarction. METHODS: Twenty-six anesthetized dogs underwent 75 minutes of left anterior descending coronary artery occlusion, followed by cardiopulmonary bypass and 60 minutes of arrest with multidose 10 degrees C BCP. In the control group (n = 8), BCP was not supplemented. In the three EMD-BCP groups, BCP was supplemented with 10 micromol/L EMD 87580 (EMD-10, n = 5), 20 micromol/L EMD 87580 (EMD-20, n = 5), or 20 micromol/L EMD 87580 combined with an immediate reperfusion bolus (5 mg/kg intravenously) (EMD-20R, n = 8). The left anterior descending coronary artery occlusion was released just before the second infusion of BCP. Reperfusion continued for 120 minutes after discontinuation of cardiopulmonary bypass. RESULTS: Postischemic systolic and diastolic function in the area at risk was dyskinetic in all groups. Infarct size (percentage of area at risk) was not significantly reduced in the EMD-10 (26.2% +/- 3.6%) and EMD-20 (22.5% +/- 2.4%) groups versus control (30.7% +/- 2.4%); however, infarct size was significantly reduced in the EMD-20R group (16.1% +/- 2.8%, p = 0.003). Edema in the area at risk in the EMD-10 (81.1% +/- 0.5% water content), EMD-20 (81.7% +/- 0.3%), and EMD-20R (81.9% +/- 0.3%) groups was less than in controls (83.2% +/- 0.2%), (p < 0.056). Neutrophil accumulation (myeloperoxidase activity) in postischemic area-at-risk myocardium was less in the EMD-20R group versus the control group (5.3 +/- 0.7 versus 8.7 +/- 1.4 absorbance units x min(-1) x g(-1); p = 0.05), which suggests an attenuated postischemic inflammatory response. CONCLUSIONS: Optimal delivery of NHE1 inhibitor to the heart through combined cardioplegia and parenteral routes significantly attenuates myocardial injury after surgical reperfusion of regional ischemia. Timing, dose, and mode of delivery of NHE1 inhibitors are important to their efficacy.

Inhibition of myocardial apoptosis reduces infarct size and improves regional contractile dysfunction during reperfusion.

OBJECTIVE: Myocardial apoptosis is primarily triggered during reperfusion (R) through various mechanisms that may involve endonuclease to cleavage genomic DNA in the internucleosomal linker regions. However, the relative contribution of myocardial apoptosis to development of myocardial injury during R remains unknown. In the present study, we examined whether inhibition of apoptosis with aurintricarboxylic acid (ATA), an endonuclease inhibitor, during R reduces infarct size and improves regional contractile function. METHODS AND RESULTS: In two groups of chronically-instrumented dogs, 1 h of left anterior descending (LAD) coronary occlusion was followed by 24 h of R with infusion of saline (control, n=8) or ATA (1 mg/kg/h, n=8) into the left atrium starting 5 min before R and continuing for 2 h. ATA significantly reduced apoptotic cells (TUNEL staining) in the peri-necrotic myocardium (12+/-1%* vs. 36+/-4%), consistent with the absence of DNA laddering. To confirm inhibition of apoptosis with ATA, densitometrically, Bcl-2 (% of normal myocardium) was significantly increased vs. control (102+/-12* vs. 68+/-9) and Bax as well as the activated caspase-3 were significantly reduced vs. control (108+/-17* vs. 194+/-42 and -29+/-4* vs. 174+/-43, respectively). ATA significantly improved segmental shortening (3.3+/-1.2* vs. -1.8+/-0.7%) and segmental work (79.3+/-11.3* vs. 7.1+/-5.8 mmHg/mm) in area at risk myocardium, and reduced infarct size (TTC staining, 27+/-0.2* vs. 37+/-0.5%), confirmed by lower plasma creatine kinase activity. In addition, myocardial blood flow (0.9+/-0.1* vs. 0.4+/-0.1 ml/min/g) and endothelial-dependent maximal vascular relaxation (119+/-6* vs. 49+/-8%) were significantly improved. Myeloperoxidase activity in area at risk myocardium, a marker for neutrophil accumulation, was also significantly reduced (17+/-4* vs. 138+/-28 Delta Abs/min). CONCLUSIONS: These data suggest that the inhibition of apoptosis during R is associated with a reduction in infarction, improvement in regional contractile and vascular endothelial functions as well as augmentation in myocardial blood flow. *P<0.05 vs. control group.

Adenosine in myocardial protection in on-pump and off-pump cardiac surgery.

Adenosine is most well known for its potent vasodilation of the vasculature. However, it also promotes glycolysis, and activates potassium-sensitive adenosine triphosphate (K(ATP)) channels. Adenosine also strongly inhibits neutrophil function such as superoxide anion production, protease release, and adherence to coronary endothelial cells. Hence adenosine attenuates ischemic injury as well as neutrophil-mediated reperfusion injury. Adenosine has also been implicated in the cardioprotective phenomenon of ischemic preconditioning. Accordingly experimental evidence shows that adenosine reduces postischemic injury when administered before ischemia and at the onset of reperfusion. Clinical studies in cardiology and cardiac surgery show cardioprotective trends with adenosine treatment but the effects are not as dramatic as those reported by experimental studies.

Blood cardioplegia supplementation with the sodium-hydrogen ion exchange inhibitor cariporide to attenuate infarct size and coronary artery endothelial dysfunction after severe regional ischemia in a canine model.

BACKGROUND: Activation of the sodium-hydrogen ion exchange mechanism results in accumulation of intracellular calcium through the sodium-calcium ion antiport mechanism. Administration of a sodium-hydrogen ion exchange inhibitor before or during ischemia attenuates myocardial ischemia and reperfusion injury. However, the cardioprotection exerted by sodium-hydrogen ion exchange inhibitors as adjuncts to cardioplegia without perioperative administration has not been tested in a model of surgical reperfusion of acute coronary occlusion with cardiopulmonary bypass. This study tested the hypothesis that sodium-hydrogen ion exchange inhibitor-supplemented blood cardioplegia would reduce postcardioplegia injury after severe regional ischemia. METHODS: In anesthetized open-chest dogs, the left anterior descending coronary artery was occluded for 75 minutes, after which total cardiopulmonary bypass was initiated. After crossclamping, cold (4 degrees C) antegrade blood cardioplegia was delivered every 20 minutes for a total of 60 minutes of cardioplegic arrest. In 8 dogs, the blood cardioplegic solution was unsupplemented (vehicle group), whereas in 8 others the solution was supplemented with the sodium-hydrogen ion exchange inhibitor cariporide (10 micro mol/L, cariporide group). RESULTS: In the in vitro studies, the direct effects of cariporide on neutrophil function were determined. Isolated canine neutrophils were stimulated by platelet activating factor. Cariporide attenuated superoxide anion production in a concentration-dependent manner, with no appreciable effect at 10 micro mol/L (the concentration used in blood cardioplegia) and a peak effect at 100 micro mol/L. In the in vivo cardiopulmonary bypass model, infarct size was significantly (P <.05) smaller in the cariporide group than in the vehicle group (22.4% +/- 3.5% vs 40.1% +/- 5.1% of area at risk), although there were no group differences in postischemic regional wall motion after 2 hours of reperfusion (0.1% +/- 0.9% vs -0.2% +/- 0.3% systolic shortening). Transmural myocardial edema in the area at risk was significantly decreased in the cariporide group (80.6% +/- 0.5%) relative to the vehicle group (83.1% +/- 0.6%). Myeloperoxidase activity in the area at risk, an index of neutrophil accumulation, was significantly lower in the cariporide group than in the vehicle group (4.7 +/- 0.9 absorbence units/[min. g tissue] vs 10.3 +/- 2.3 absorbence units/[min. g tissue]). In isolated postischemic left anterior descending coronary artery rings, maximum relaxation in response to the endothelium-dependent vasodilator acetylcholine was significantly greater in the cariporide group than in the vehicle group (77.5% +/- 7.4% vs 51.4% +/- 8.0%), whereas smooth muscle relaxation in response to nitroprusside was comparable between groups. CONCLUSION: In this canine model, supplementation of blood cardioplegia with cariporide, a sodium-hydrogen ion exchange inhibitor, reduced infarct size, attenuated neutrophil accumulation in the area at risk, and reduced postischemic coronary artery endothelial dysfunction without directly inhibiting neutrophil activity. Cariporide as an adjunct to blood cardioplegia without perioperative administration attenuated surgical ischemia-reperfusion injury in jeopardized myocardium.

One hundred pulmonary valve replacements in children after relief of right ventricular outflow tract obstruction.

BACKGROUND: Surgical repair of obstructive lesions of the right ventricular outflow tract (RVOT) in children commonly creates pulmonary valve incompetence that may eventually require pulmonary valve replacement (PVR). We reviewed our experience with PVR late after RVOT reconstruction. METHODS: We performed 100 PVRs in 93 children 1.1 months to 22.4 years (median 8) after RVOT reconstruction. Children with right ventricular to pulmonary artery conduits and primary PVRs were excluded. Age at PVR was 4.5 months to 27.9 years (median 9.5 years). Initial diagnosis was tetralogy of Fallot and variants, 62; critical pulmonary stenosis, 15; pulmonary atresia with intact ventricular septum, 7; and others, 9. Eleven patients had a redo PVR. A total of 62 PVRs were homografts; 38 were porcine valves. RESULTS: There was one early death. On follow-up of 5 months to 12.4 years (mean 4.9 years) there were no late deaths although 1 child underwent cardiac transplantation. Actuarial freedom from redo PVR at 8 years was 100% for porcine valves but 70% for homograft valves (p = 0.17). For children younger than 3 years at PVR, freedom from reoperation was 76% at 1 year and 39% at 8 years compared with freedom from redo PVR at 8 years of 100% for children older than 3 years. On latest echocardiogram 97% of porcine valves had mild or no pulmonary regurgitation compared with 72% of homograft valves. CONCLUSIONS: PVR after RVOT reconstruction can be performed with low risk. Porcine valves may be superior to homograft valves although this advantage may be due to older age at time of PVR.

Preserved myocardial blood flow and oxygen supply-demand balance with active coronary perfusion during simulated off-pump coronary artery bypass grafting.

BACKGROUND: During off-pump coronary artery bypass surgery, concern remains about the possible myocardial injury associated with the transient occlusion and stabilization of the target vessels. Although intraluminal shunts are used to avoid ischemia during graft anastomosis, blood flow through the shunts can be affected by upstream pressure and inherent resistance, resulting in reduced blood flow during hypotension or severe proximal stenosis. METHODS: In anesthetized dogs regional myocardial blood flow (microspheres), oxygen consumption, lactate extraction, and systolic shortening (sonomicrometry) were measured in the myocardium served by the left anterior descending coronary artery with native perfusion after interposition of a 2.25-mm shunt (> or = 90% of left anterior descending diameter) and during active coronary perfusion with a constant flow pump. Measurements were made under normotension and hypotension produced by partial caval occlusion to reduce arterial pressure by 50%. RESULTS: Interposition of the shunt reduced blood flow by 67.8%, regional oxygen delivery by 59.8%, and systolic shortening by 45.6% relative to baseline, but lactate extraction (31.0% vs 31.2%) and oxygen supply-consumption (O(2)S/myocardial oxygen consumption ratio, 2.7 +/- 0.5 vs 2.6 +/- 0.5) were comparable with baseline values. Hypotension further decreased these physiologic values and was associated with local lactate production (-67.4% extraction) and decreased O(2)S/myocardial oxygen consumption ratio (1.3 +/- 0.1). Active coronary perfusion was associated with regional blood flow, oxygen delivery, systolic shortening, and lactate extraction comparable with baseline values. In contrast to the shunt, active perfusion maintained myocardial flow, oxygen delivery, and lactate extraction during hypotension and normalized the O(2)S/myocardial oxygen consumption ratio, although systolic shortening decreased as a result of ventricular unloading. CONCLUSION: Intraluminal shunts may impede oxygen delivery to the target myocardium, which precipitates regional ischemia during transient hypotension. Active coronary perfusion provides adequate oxygen supply independent of systemic blood pressure.

Palliative management of malignant airway obstruction.

BACKGROUND: Obstruction of the airway due to unresectable malignant disease is a frightening condition that portends a poor prognosis. Endobronchial treatment modalities were reviewed to determine the most effective management strategy. METHODS: A 12-year retrospective review (1988 to 1999) of 121 consecutive patients with inoperable malignant airway obstruction (MAO) was performed. Sixty-five patients received high-dose-rate brachytherapy (HDR) alone, 32 received HDR plus neodymium:yttrium-aluminum garnet laser (YAG) therapy, 16 received YAG only, 4 patients were stented, and 4 received photodynamic therapy (PDT). Follow-up was obtained by chart review and contact. RESULTS: Seventy-seven men and 44 women, median age 62 years (range 30 to 86 years), underwent 378 endobronchial procedures for relief of MAO. Good to excellent results were achieved in 77% (93/121) of patients. Seventy-two percent (23/32) of patients undergoing HDR plus YAG received a good to excellent result. All 8 patients receiving either stents or PDT had good to excellent palliation. There were no intraoperative deaths, but there were two in-hospital deaths. Complications occurred in 4% (5/121) of patients. Forty-four percent (53/121) of our patients were lost to follow-up. Mean survival was 6.7 months after the last treatment. CONCLUSIONS: Temporary relief of inoperable MAO can be accomplished with a number of endobronchial treatments used either singularly or in combination. The majority of patients managed with HDR, YAG, or HDR plus YAG received good to excellent short-term palliation.